Thrombin-activatable fibrinolysis inhibitor protects against acute lung injury by inhibiting the complement system
Acute lung injury (ALI) is a devastating disease with an overall mortality rate of 30 to 40%. The coagulation/fibrinolysis system is implicated in the pathogenesis of ALI. Thrombin-activatable fibronolysis inhibitor (TAFI) is an important component of the fibrinolysis system. Recent studies have sho...
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| Veröffentlicht in: | American journal of respiratory cell and molecular biology 2013-10, Vol.49 (4), p.646-653 |
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| creator | Naito, Masahiro Taguchi, Osamu Kobayashi, Tetsu Takagi, Takehiro D'Alessandro-Gabazza, Corina N Matsushima, Yuki Boveda-Ruiz, Daniel Gil-Bernabe, Paloma Matsumoto, Takahiro Chelakkot-Govindalayathil, Ayshwarya-Lakshmi Toda, Masaaki Yasukawa, Atsushi Hataji, Osamu Morser, John Takei, Yoshiyuki Gabazza, Esteban C |
| description | Acute lung injury (ALI) is a devastating disease with an overall mortality rate of 30 to 40%. The coagulation/fibrinolysis system is implicated in the pathogenesis of ALI. Thrombin-activatable fibronolysis inhibitor (TAFI) is an important component of the fibrinolysis system. Recent studies have shown that the active form of TAFI can also regulate inflammatory responses by its ability to inhibit complement C3a, C5a, and osteopontin. We hypothesized that TAFI might have a protective role in ALI. To demonstrate this hypothesis, the development of ALI was compared between wild-type (WT) and TAFI-deficient mice. ALI was induced by intratracheal instillation of LPS. Control mice were treated with saline. Animals were killed 24 hours after LPS. The number of inflammatory cells and the concentration of total protein and inflammatory cytokines were significantly increased in bronchoalveolar lavage fluid from LPS-treated, TAFI-deficient mice compared with their WT counterparts. Significantly higher concentrations of C5a were found in bronchoalveolar lavage fluid and plasma in LPS-treated TAFI knockout mice compared with WT mice. Pretreatment with inhaled C5a receptor antagonist blocked the detrimental effects of TAFI deficiency to levels found in WT mice. Our results show that TAFI protects against ALI, at least in part, by inhibiting the complement system. |
| doi_str_mv | 10.1165/rcmb.2012-0454OC |
| format | Article |
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The coagulation/fibrinolysis system is implicated in the pathogenesis of ALI. Thrombin-activatable fibronolysis inhibitor (TAFI) is an important component of the fibrinolysis system. Recent studies have shown that the active form of TAFI can also regulate inflammatory responses by its ability to inhibit complement C3a, C5a, and osteopontin. We hypothesized that TAFI might have a protective role in ALI. To demonstrate this hypothesis, the development of ALI was compared between wild-type (WT) and TAFI-deficient mice. ALI was induced by intratracheal instillation of LPS. Control mice were treated with saline. Animals were killed 24 hours after LPS. The number of inflammatory cells and the concentration of total protein and inflammatory cytokines were significantly increased in bronchoalveolar lavage fluid from LPS-treated, TAFI-deficient mice compared with their WT counterparts. Significantly higher concentrations of C5a were found in bronchoalveolar lavage fluid and plasma in LPS-treated TAFI knockout mice compared with WT mice. Pretreatment with inhaled C5a receptor antagonist blocked the detrimental effects of TAFI deficiency to levels found in WT mice. Our results show that TAFI protects against ALI, at least in part, by inhibiting the complement system.</description><identifier>ISSN: 1044-1549</identifier><identifier>EISSN: 1535-4989</identifier><identifier>DOI: 10.1165/rcmb.2012-0454OC</identifier><identifier>PMID: 23721130</identifier><language>eng</language><publisher>United States: American Thoracic Society</publisher><subject>Acute Lung Injury - immunology ; Acute Lung Injury - metabolism ; Animals ; Blood Coagulation - immunology ; Bronchoalveolar Lavage Fluid - immunology ; Carboxypeptidase B2 - deficiency ; Carboxypeptidase B2 - metabolism ; Complement C5a - immunology ; Complement C5a - metabolism ; Cytokines - immunology ; Cytokines - metabolism ; Fibrinolysis - immunology ; Inflammation - immunology ; Inflammation - metabolism ; Lipopolysaccharides - immunology ; Lung - immunology ; Lung - metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neutrophils - immunology ; Neutrophils - metabolism ; Pneumonia - immunology ; Pneumonia - metabolism ; Thrombin - immunology ; Thrombin - metabolism</subject><ispartof>American journal of respiratory cell and molecular biology, 2013-10, Vol.49 (4), p.646-653</ispartof><rights>Copyright American Thoracic Society Oct 2013</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c476t-e4dfc24fcfcb5db4fb15aaff2f1a57bd2d2a60c113b9031705eb1709af5288493</citedby><cites>FETCH-LOGICAL-c476t-e4dfc24fcfcb5db4fb15aaff2f1a57bd2d2a60c113b9031705eb1709af5288493</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23721130$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Naito, Masahiro</creatorcontrib><creatorcontrib>Taguchi, Osamu</creatorcontrib><creatorcontrib>Kobayashi, Tetsu</creatorcontrib><creatorcontrib>Takagi, Takehiro</creatorcontrib><creatorcontrib>D'Alessandro-Gabazza, Corina N</creatorcontrib><creatorcontrib>Matsushima, Yuki</creatorcontrib><creatorcontrib>Boveda-Ruiz, Daniel</creatorcontrib><creatorcontrib>Gil-Bernabe, Paloma</creatorcontrib><creatorcontrib>Matsumoto, Takahiro</creatorcontrib><creatorcontrib>Chelakkot-Govindalayathil, Ayshwarya-Lakshmi</creatorcontrib><creatorcontrib>Toda, Masaaki</creatorcontrib><creatorcontrib>Yasukawa, Atsushi</creatorcontrib><creatorcontrib>Hataji, Osamu</creatorcontrib><creatorcontrib>Morser, John</creatorcontrib><creatorcontrib>Takei, Yoshiyuki</creatorcontrib><creatorcontrib>Gabazza, Esteban C</creatorcontrib><title>Thrombin-activatable fibrinolysis inhibitor protects against acute lung injury by inhibiting the complement system</title><title>American journal of respiratory cell and molecular biology</title><addtitle>Am J Respir Cell Mol Biol</addtitle><description>Acute lung injury (ALI) is a devastating disease with an overall mortality rate of 30 to 40%. The coagulation/fibrinolysis system is implicated in the pathogenesis of ALI. Thrombin-activatable fibronolysis inhibitor (TAFI) is an important component of the fibrinolysis system. Recent studies have shown that the active form of TAFI can also regulate inflammatory responses by its ability to inhibit complement C3a, C5a, and osteopontin. We hypothesized that TAFI might have a protective role in ALI. To demonstrate this hypothesis, the development of ALI was compared between wild-type (WT) and TAFI-deficient mice. ALI was induced by intratracheal instillation of LPS. Control mice were treated with saline. Animals were killed 24 hours after LPS. The number of inflammatory cells and the concentration of total protein and inflammatory cytokines were significantly increased in bronchoalveolar lavage fluid from LPS-treated, TAFI-deficient mice compared with their WT counterparts. Significantly higher concentrations of C5a were found in bronchoalveolar lavage fluid and plasma in LPS-treated TAFI knockout mice compared with WT mice. Pretreatment with inhaled C5a receptor antagonist blocked the detrimental effects of TAFI deficiency to levels found in WT mice. Our results show that TAFI protects against ALI, at least in part, by inhibiting the complement system.</description><subject>Acute Lung Injury - immunology</subject><subject>Acute Lung Injury - metabolism</subject><subject>Animals</subject><subject>Blood Coagulation - immunology</subject><subject>Bronchoalveolar Lavage Fluid - immunology</subject><subject>Carboxypeptidase B2 - deficiency</subject><subject>Carboxypeptidase B2 - metabolism</subject><subject>Complement C5a - immunology</subject><subject>Complement C5a - metabolism</subject><subject>Cytokines - immunology</subject><subject>Cytokines - metabolism</subject><subject>Fibrinolysis - immunology</subject><subject>Inflammation - immunology</subject><subject>Inflammation - metabolism</subject><subject>Lipopolysaccharides - immunology</subject><subject>Lung - immunology</subject><subject>Lung - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Neutrophils - 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Academic</collection><jtitle>American journal of respiratory cell and molecular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Naito, Masahiro</au><au>Taguchi, Osamu</au><au>Kobayashi, Tetsu</au><au>Takagi, Takehiro</au><au>D'Alessandro-Gabazza, Corina N</au><au>Matsushima, Yuki</au><au>Boveda-Ruiz, Daniel</au><au>Gil-Bernabe, Paloma</au><au>Matsumoto, Takahiro</au><au>Chelakkot-Govindalayathil, Ayshwarya-Lakshmi</au><au>Toda, Masaaki</au><au>Yasukawa, Atsushi</au><au>Hataji, Osamu</au><au>Morser, John</au><au>Takei, Yoshiyuki</au><au>Gabazza, Esteban C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Thrombin-activatable fibrinolysis inhibitor protects against acute lung injury by inhibiting the complement system</atitle><jtitle>American journal of respiratory cell and molecular biology</jtitle><addtitle>Am J Respir Cell Mol Biol</addtitle><date>2013-10-01</date><risdate>2013</risdate><volume>49</volume><issue>4</issue><spage>646</spage><epage>653</epage><pages>646-653</pages><issn>1044-1549</issn><eissn>1535-4989</eissn><abstract>Acute lung injury (ALI) is a devastating disease with an overall mortality rate of 30 to 40%. The coagulation/fibrinolysis system is implicated in the pathogenesis of ALI. Thrombin-activatable fibronolysis inhibitor (TAFI) is an important component of the fibrinolysis system. Recent studies have shown that the active form of TAFI can also regulate inflammatory responses by its ability to inhibit complement C3a, C5a, and osteopontin. We hypothesized that TAFI might have a protective role in ALI. To demonstrate this hypothesis, the development of ALI was compared between wild-type (WT) and TAFI-deficient mice. ALI was induced by intratracheal instillation of LPS. Control mice were treated with saline. Animals were killed 24 hours after LPS. The number of inflammatory cells and the concentration of total protein and inflammatory cytokines were significantly increased in bronchoalveolar lavage fluid from LPS-treated, TAFI-deficient mice compared with their WT counterparts. Significantly higher concentrations of C5a were found in bronchoalveolar lavage fluid and plasma in LPS-treated TAFI knockout mice compared with WT mice. Pretreatment with inhaled C5a receptor antagonist blocked the detrimental effects of TAFI deficiency to levels found in WT mice. Our results show that TAFI protects against ALI, at least in part, by inhibiting the complement system.</abstract><cop>United States</cop><pub>American Thoracic Society</pub><pmid>23721130</pmid><doi>10.1165/rcmb.2012-0454OC</doi><tpages>8</tpages></addata></record> |
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| ispartof | American journal of respiratory cell and molecular biology, 2013-10, Vol.49 (4), p.646-653 |
| issn | 1044-1549 1535-4989 |
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| source | Journals@Ovid Ovid Autoload; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Acute Lung Injury - immunology Acute Lung Injury - metabolism Animals Blood Coagulation - immunology Bronchoalveolar Lavage Fluid - immunology Carboxypeptidase B2 - deficiency Carboxypeptidase B2 - metabolism Complement C5a - immunology Complement C5a - metabolism Cytokines - immunology Cytokines - metabolism Fibrinolysis - immunology Inflammation - immunology Inflammation - metabolism Lipopolysaccharides - immunology Lung - immunology Lung - metabolism Male Mice Mice, Inbred C57BL Mice, Knockout Neutrophils - immunology Neutrophils - metabolism Pneumonia - immunology Pneumonia - metabolism Thrombin - immunology Thrombin - metabolism |
| title | Thrombin-activatable fibrinolysis inhibitor protects against acute lung injury by inhibiting the complement system |
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